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Separating Fluid Shear Stress from Acceleration during Vibrations in Vitro: Identification of Mechanical Signals Modulating the Cellular Response

机译:在振动过程中体外分离加速流体剪切力:机械信号调制的细胞反应的鉴定

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摘要

The identification of the physical mechanism(s) by which cells can sense vibrations requires the determination of the cellular mechanical environment. Here, we quantified vibration-induced fluid shear stresses in vitro and tested whether this system allows for the separation of two mechanical parameters previously proposed to drive the cellular response to vibration – fluid shear and peak accelerations. When peak accelerations of the oscillatory horizontal motions were set at 1g and 60Hz, peak fluid shear stresses acting on the cell layer reached 0.5Pa. A 3.5-fold increase in fluid viscosity increased peak fluid shear stresses 2.6-fold while doubling fluid volume in the well caused a 2-fold decrease in fluid shear. Fluid shear was positively related to peak acceleration magnitude and inversely related to vibration frequency. These data demonstrated that peak shear stress can be effectively separated from peak acceleration by controlling specific levels of vibration frequency, acceleration, and/or fluid viscosity. As an example for exploiting these relations, we tested the relevance of shear stress in promoting COX-2 expression in osteoblast like cells. Across different vibration frequencies and fluid viscosities, neither the level of generated fluid shear nor the frequency of the signal were able to consistently account for differences in the relative increase in COX-2 expression between groups, emphasizing that the eventual identification of the physical mechanism(s) requires a detailed quantification of the cellular mechanical environment.
机译:细胞可以感测振动的物理机制的鉴定需要确定细胞机械环境。这里,我们在体外量化振动诱导的流体剪切应力并测试该系统是否允许先前提出的两个机械参数分离以驱动振动流体剪切和峰值加速度的蜂窝响应。当振荡水平运动的峰值加速设定为1G和60Hz时,作用在电池层上的峰流体剪切应力达到0.5Pa。流体粘度增加3.5倍,增加峰流体剪切应力2.6倍,同时井中的液体体积加倍,导致流体剪切的2倍降低。流体剪切与峰值加速度呈正相关,与振动频率相反。这些数据证明,通过控制特定的振动频率,加速度和/或流体粘度,可以有效地与峰加速度有效地分离峰值剪切应力。作为利用这些关系的示例,我们测试了剪切应力在促进成骨细胞中促进Cox-2表达的剪切应力。跨越不同的振动频率和流体粘度,所产生的流体剪切的水平和信号的频率都不能够一致地考虑组之间的COX-2表达的相对增加的差异,强调物理机制的最终识别( S)需要详细定量细胞机械环境。

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